The Intersection of Cutaneous Lupus and Osteonecrosis: Dermatologic Implications for Orthopedic Joint Preservation  

作　　者：Alejandra Sataray-Rodriguez Janae Rasmussen Klaudia Greer Shivam Shah Vivian Liang Laura Palma Kelly Frasier Pedram Razavi Garrett Chin Alejandra Sataray-Rodriguez;Janae Rasmussen;Klaudia Greer;Shivam Shah;Vivian Liang;Laura Palma;Kelly Frasier;Pedram Razavi;Garrett Chin(Reno School of Medicine, University of Nevada, Reno, NV, USA;Valley Consortium for Medical Education, Modesto, CA, USA;Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA;Health Sciences Center at Shreveport, School of Medicine, Louisiana State University, Shreveport, LA, USA;School of Osteopathic Medicine in Arizona, A.T. Still University, Mesa, AZ, USA;SUNY Upstate Medical University, Syracuse, NY, USA;Department of Dermatology, Northwell Health, New Hyde Park, NY, USA)

机构地区：[1]Reno School of Medicine, University of Nevada, Reno, NV, USA [2]Valley Consortium for Medical Education, Modesto, CA, USA [3]Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA [4]Health Sciences Center at Shreveport, School of Medicine, Louisiana State University, Shreveport, LA, USA [5]School of Osteopathic Medicine in Arizona, A.T. Still University, Mesa, AZ, USA [6]SUNY Upstate Medical University, Syracuse, NY, USA [7]Department of Dermatology, Northwell Health, New Hyde Park, NY, USA

出　　处：《Modern Research in Inflammation》2024年第4期43-57,共15页炎症(英文)

摘　　要：The intersection of cutaneous lupus erythematosus (CLE) and osteonecrosis highlights a complex relationship between dermatologic and orthopedic pathology, underscoring the systemic nature of autoimmune disease. Osteonecrosis, characterized by ischemic bone death and subsequent joint degeneration, is a known complication in systemic lupus erythematosus (SLE), but emerging evidence suggests that CLE manifestations may serve as early indicators or contributory factors in its development. Chronic inflammation and microvascular injury, central to CLE pathophysiology, may predispose affected patients to compromised bone perfusion and ischemia, particularly in weight-bearing joints such as the hips and knees. Dermatologic signs, including persistent erythema, ulceration, or livedo reticularis, may reflect underlying vascular dysfunction that extends beyond the skin to subchondral bone, accelerating osteonecrotic processes. The role of autoantibodies, such as antiphospholipid antibodies, and their contribution to thrombotic microangiopathy in CLE further supports this potential mechanistic link. Early recognition of CLE-related vascular changes could guide orthopedic surveillance strategies, enabling timely imaging with MRI to detect early osteonecrosis before irreversible joint damage occurs. Therapeutic interventions for CLE, including corticosteroids and immunosuppressive agents, may inadvertently exacerbate osteonecrosis risk, necessitating careful balancing of treatment efficacy with preservation of joint health. Advances in vascular-targeted therapies and bone-preserving interventions, such as bisphosphonates or regenerative techniques, offer potential avenues for mitigating joint degeneration in this patient population. Understanding the bidirectional relationship between CLE and osteonecrosis provides an opportunity for dermatologists and orthopedists to collaborate on predictive, preventive, and therapeutic strategies that preserve joint function and improve quality of life for affected individuals.The intersection of cutaneous lupus erythematosus (CLE) and osteonecrosis highlights a complex relationship between dermatologic and orthopedic pathology, underscoring the systemic nature of autoimmune disease. Osteonecrosis, characterized by ischemic bone death and subsequent joint degeneration, is a known complication in systemic lupus erythematosus (SLE), but emerging evidence suggests that CLE manifestations may serve as early indicators or contributory factors in its development. Chronic inflammation and microvascular injury, central to CLE pathophysiology, may predispose affected patients to compromised bone perfusion and ischemia, particularly in weight-bearing joints such as the hips and knees. Dermatologic signs, including persistent erythema, ulceration, or livedo reticularis, may reflect underlying vascular dysfunction that extends beyond the skin to subchondral bone, accelerating osteonecrotic processes. The role of autoantibodies, such as antiphospholipid antibodies, and their contribution to thrombotic microangiopathy in CLE further supports this potential mechanistic link. Early recognition of CLE-related vascular changes could guide orthopedic surveillance strategies, enabling timely imaging with MRI to detect early osteonecrosis before irreversible joint damage occurs. Therapeutic interventions for CLE, including corticosteroids and immunosuppressive agents, may inadvertently exacerbate osteonecrosis risk, necessitating careful balancing of treatment efficacy with preservation of joint health. Advances in vascular-targeted therapies and bone-preserving interventions, such as bisphosphonates or regenerative techniques, offer potential avenues for mitigating joint degeneration in this patient population. Understanding the bidirectional relationship between CLE and osteonecrosis provides an opportunity for dermatologists and orthopedists to collaborate on predictive, preventive, and therapeutic strategies that preserve joint function and improve quality of life for affected individuals.

关 键 词：Cutaneous Lupus Erythematosus OSTEONECROSIS Systemic Lupus Erythematosus Autoimmune Disease Chronic Inflammation Microvascular Injury 

分 类 号：R73[医药卫生—肿瘤]